Although it is tempting to assume that the passing-on of maternal immune memory would convey an evolutionary advantage, the only well established mechanism consists of the temporary protection of neonates by maternal IgG antibodies carried across the placenta, or, in animals but not humans, antibody coating of enterocyte surfaces during lactation (Zinkernagel, R. M., Maternal antibodies, childhood infections, and autoimmune diseases. N. Engl. J. Med. 345, 1331-1335 (2001)). All other active humoral immune defenses are thought to depend on mature B and T cells and to require “learning”, i.e. clonal expansion of antigen-specific lymphocytes (Abbas et al., Cellular and Molecular Immunology (Elsevier, 2005); Germain, Nat. Med. 10: 1307-20 (2004)), with the possible exception of B-1 cell derived natural IgM antibodies that convey protection against a limited repertoire of bacterial antigens (Kantor et al., J. Immunol. 158, 1175-1186 (1997); Hayakawa et al. Science 285, 113-116 (1999)).